![]() ![]() Macrophages can be divided into two polarization states of classically activated M1 macrophages and alternatively activated M2 macrophages under different microenvironments. ![]() The main features of synovitis are synovial tissue hyperplasia, inner macrophage aggregation, and cell secretory dysfunction. Synovitis is closely related to the polarization of synovial macrophages. The synovial sub-lining layer consists of blood vessels, fibrous connective tissue, macrophages, and a small number of lymphocytes. The intimal lining is composed of two to three layers of synovial cells, including macrophage-like cells, fibroblast-like cells, dendrite-like synoviocytes, and a few mesenchymal stem cells. The normal synovium can be divided into an intimal lining layer and a synovial sub-lining layer. The synovial membrane is thin, soft, loose connective tissue that is coated on the inner side of the joint capsule and forms a closed capsule around the joint cavity. Synovial inflammation is associated with the pathogenesis of OA and is significantly associated with the severity of OA. Therefore, to determine the pathogenesis of OA, effective intervention in the early stages of pathogenesis is a key step for successful treatment. The incidence of OA in the middle-aged population can be as high as 40%-80%, and the disability rate is greater than 50%, which imparts a substantial burden to individuals and society. However, complications such as the necessity to wear prostheses and loosening of artificial joints greatly limit the application of artificial joint replacement. Advanced OA is often treated with artificial joint replacement, which can relieve pain and restore patients’ daily living abilities. However, those measures can only alleviate the clinical symptoms and cannot prevent the development of disease thus, the effect is not satisfactory. At present, the clinical treatment of early OA includes the use of anti-inflammatory analgesic drugs, the application of chondroprotective drugs, and arthroscopic debridement, among other approaches. After the degeneration of cartilage, degradation products cause inflammation in the joints, which are accompanied by changes in subchondral bone and the synovium. Articular cartilage is a component of the articular surface that acts as a buffer, allowing fluid flow and the dispersion of pressure. Imbalances in the synthesis of articular chondrocytes, extracellular matrix, and subchondral bone is a pathological feature during degradation. The pathogenesis of OA results in the degeneration of chondrocytes and cartilage. Osteoarthritis (OA) is a degenerative joint disease that seriously affects cartilage and surrounding tissues. Our results demonstrated that bone marrow mesenchymal stem cell-derived exosomes may relieve osteoarthritis by promoting the phenotypic transformation of synovial macrophages from M1 to M2. In vitro, macrophages treated with exosomes maintain chondrocytes’ chondrogenic characteristics and inhibit hypertrophy. In synovial fluid, the expression levels of the proinflammatory cytokines, IL-1β, IL-6, and TNF-α were decreased and the release of the anti-inflammatory cytokine, IL-10 was increased. Exosomes alleviate cartilage damage, reduce osteophyte formation and synovial macrophage infiltration, inhibit M1 macrophage production and promote M2 macrophage generation. We demonstrated that bone marrow mesenchymal stem cell-derived exosomes can delay the progression of osteoarthritis. Exosomes are also important carriers of paracrine delivery agents and promote communication between cells. Exosomes are the smallest known membrane-bound nanovesicles. Research has shown that the paracrine mechanism is the main mode of action of mesenchymal stem cells. Bone marrow mesenchymal stem cells can repair cartilage damage and treat osteoarthritis via cell therapies or in-tissue engineering. Osteoarthritis is a chronic degenerative disease that can lead to restricted activity or even disability. ![]()
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